CSF, Hydrocephalus and LP Flashcards

1
Q

Definition of hydrocephalus

A

A general condition whereby there is an excess CSF within the intracranial space and specifically, the intraventricular spaces within the brain - causing dilatation of the ventricles and a wide range of symptoms

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2
Q

Where is the majority of CSF produced by?

A

Choroid plexus

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3
Q

How is CSF produced?

A

Metabolically active process within the brain (requires ATP) whereby sodium is pumped into the subarachnoid space, and water follows from the blood vessels

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4
Q

Where is choroid plexus located?

A
Lateral ventricles
- temporal horn roofs
- floor of bodies
Posterior 3rd ventricle roof
Caudal 4th ventricle roof
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5
Q

Where is the biggest choroid plexus found?

A

Lateral ventricle

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6
Q

What is the mechanism of CSF flow?

A

Flows from the two lateral ventricles into the 3rd ventricle (through the foramen of munro) then down the aqueduct into the 4th ventricle.
Then out through the megendie foramen (single and midline) and two Luschcka foramen (lateral)
After exiting the 4th ventricle, flows through subarachnoid space over and around the brain and spinal cord and is eventually reabsorbed into the venous system through numerous arachnoid granulations along the dural venous sinuses (esp the superior sagital sinus

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7
Q

How many cc’s does an average adult brain produce?

A

450 - 600 ccs

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8
Q

Normally, production of CSF = what?

A

Resorption of CSF

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9
Q

What do arachnoid granulations contain?

A

Arachnoid villi

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10
Q

Two types of hydrocephalus

A
Communicating hydrocephalus (CoH)
Non communicating hydrocephalus (NCH)
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11
Q

What is communicating hydrocephalus also known as?

A

Non obstructive hydrocephalus

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12
Q

What is non communicating hydrocephalus also known as?

A

Obstructive hydrocephalus

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13
Q

What is communicating hydrocephalus?

A

CSF pathway open from “start to finish”, meaning CSF can travel freely from the choroid plexus to the arachnoid granulations, then you have “no obstruction” and a communicating hydrocephalus

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14
Q

What is non communicating hydrocephalus?

A

If CSF cannot travel freely from start to finish, then youve got an “obstruction” and non communicating hydrocephalus

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15
Q

What does communicating hydrocephalus usually represent a problem with?

A

CSF reabsorption - which cannot keep up with the rate of CSF production

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16
Q

Result of communicating hydrocephalus

A

As the ventricular system dilates uniformly, the ICP rises

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17
Q

Pathology of communicating hydrocephalus

A

Underabsorption of CSF

Overproduction of CSF (RARE)

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18
Q

Presentation of communicating hydrocephalus

A

Young children whose sutures havent fused yet
- disproportional increased in head circumference
- failure to thrive
Children with fused sutures / adults
- symptoms of increased ICP; Headache, nausea and vomiting, gait distrubance, 6th cranial nerve palsy, papilloedema, upgaze difficulty

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19
Q

Causes of Communicating hydrocephalus

A

Infection (e.g. bacterial meningitis)
Subarachnoid haemorrhage (blood and blood breakdown products cause scarring of arachnoid granulations)
Post op
Head trauma

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20
Q

Causes of non communicating hydrocephalus

A
Aqueductal stenosis
Tumours / cancers / metastases
Cysts
Infection 
Haemorrhage/haematoma 
Congenital malformations/conditions
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21
Q

How quickly do the symptoms of non communicating hydrocephalus come on?

A
Processes that have developed over long periods of time - more gradual symptoms (i.e. masses etc)
Acute processes (i.e. intraventricular bleed) can cause acute obstruction with rapid mental status decline
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22
Q

What is the earliest radiographic finding of non communicating hydrocephalus?

A

Dilatation of temporal horns of the lateral ventricles

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23
Q

Radiographic findings of non communicating hydrocephalus

A

First dilatation of temporal horns
Third ventricle becomes ballooned
Lateral ventricle will increase in size
Peripheral sulci effaced

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24
Q

An evans ratio greater than or equal to 0.3 defines what?

A

Ventriculomegaly

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25
Treatment of acute hydrocephalus
Urgent or emergency placement of extra ventricular drain (EVD)
26
How does an EVD work?
Catheter passed through the patient's scalp and skull into the lateral ventricle, that drains CSF to a collecting system kept at the patients bedside
27
Treatment of communicating hydrocephalus
Shunt placement
28
Types of shunt used to treat communicating hydrocephalus
Ventriculo-peritoneal Lumbar peritoneal Ventricular atrio
29
What is the most common type of shunt used in communicating hydrocephalus?
Ventriculo-peritoneal shunt
30
Treatment of non communicating hydrocephalus
Removing obstructive lesion +/- Shunt Possibly a third ventriculostomy
31
How does a third ventriculostomy work?
Often performed in conjunction with BP shunt placement Hole is opened surgically in the floor of the third ventricle so CSF flows out into the interpeduncular cistern and pre-pontine space (bypasses cerebral aqueduct)
32
Causes of VP shunt failure
``` Mechanical failure from occlusion/disconnection Migration Overdrainage/underdrainage Infection Skin erosion ```
33
What % of shunts fail 5 years after placement?
50%
34
What % of shunts can fail in the first year?
40%
35
What does NPH stand for?
Normal pressure hydrocephalus
36
What is NPH a rare preventable cause of?
Dementia
37
Classic triad of NPH
Wet, wobbly and wacky
38
Presentation of NPH
``` Urinary incontinence Gait disturbance - wide stance - short, shuffling steps Quickly progressive dementia ```
39
What is usually the first symptom to present of NPH?
Gait disturbance
40
Investigations of NPH
CT/MRI LP - normal opening pressure
41
What do symptoms of NPH improve with?
CSF removal
42
Treatment of NPH
VP shunt placement
43
Prognosis of NPH
Outcome improved if symptoms been present for shorter period of time
44
What is the least likely symptom of NPH to improve with shunting?
Dementia
45
What position should the patient be in for LP?
Lateral decubitus position
46
What level does the spinal cord end?
L1-L2
47
What level are LPs done at?
L3-L4 or L4-L5
48
What position are infants held in for LP?
Seated position with maximal spinal flexion
49
Indications for LP; to obtain CSF for the diagnosis of.....
``` Meningitis (WCC) Meningoencephalitis (WCC) SAH (bilirubin) Malignancy Idiopathic intracranial HTN Other neurological syndromes Infusion (e.g. NPH studies) of drugs or contrast ```
50
Contraindications for LP
Unstable patient with CVS or Resp system instability Localized skin/soft tissue infection over puncture site Evidence of unstable bleeding disorder Platelets < 50,000 or clotting factor deficiency For bleeding diathesis Increased intracranial pressure Caution in patients with chiari malformations
51
Complications of LP
``` Headache Apnea Back pain Bleeding or fluid leak around the spinal cord Infection Pain Haematoma Ocular muscle palsy (transient) Nerve trauma Brainstem herniation Subarachnoid epidermal cyst ```
52
Who is headache after LP uncommon in?
< 10 y/o
53
What is the most common complication of LP?
Spinal headache
54
Risk factors for spinal headache post LP
``` Female Age 18-30 Lower BMI History of Headache Prior spinal headache ```
55
Features of spinal headache post LP
Bilateral | Improves when supine
56
Treatment of spinal headache post LP
Supine position for at least 2 hours Hydration Caffeine either PO or IV Epidural blood patch
57
Prevention of spinal headache
Passing needle bevel parallel to longitudinal fibres of the dura Replacing stylet before removing needle Using smaller diameter needes Using atraumatic needles
58
Presentation of nerve root trauma/irritation
Electric shocks Dysesthesias Back pain persistent for months
59
If cause nerve root irritation during LP, what should be done?
Withdraw needle immediately | If pain or motor weakness persists, start corticosteriods
60
What should be scheduled if nerve root pain continues after trauma?
Electromyogram/nerve conduction velocity studies
61
What does brain herniation manifest as?
Altered mental status Followed by cranial nerve abnormalities Cushings triad May be rapidly fatal
62
Treatment of brain herniation due to LP
Immediately remove the needle and raise the head of the bed to 30 - 45 degrees to improve venous return from the brain Mannitol or 3% saline Intubate patient and ventilate Emergency neurosurgical consult
63
When does an epidual inclusion cyst occur?
Occurs when a core of skin is driven into spinal or paraspinal space with a hollow needle Rare due to use of stylet
64
What does CSF look like?
Clear | Colourless
65
Opening pressure of CSF
6 - 16 MM/H20
66
Protein level of CSF
35%
67
Glucose level of CSF
60%
68
WCC of CSF
< 5
69
Who is idiopathic intracranial HTN often seen in?
Young, overweight females
70
Risk factors for idiopathic intracranial HTN
Obesity Female Pregnancy Drugs - OCP, sterioids, tetracycline, vit A, lithium
71
Presentation of idiopathic intracranial HTN
``` Headache Blurred vision Papilloedema Enlarged blind spot Sixth nerve palsy may be present ```
72
Treatment of idiopathic intracranial HTN
``` Weight loss Diuretics Topiramate Repeated LP Surgery - to prevent optic nerve damage (decompression of optic nerve and fenestration) and can also insert a shunt ```
73
What is normal pressure hydrocephalus a reversible cause of in the elderly?
Dementia
74
What is normal pressure hydrocephalus secondary to? What else could it be secondary to?
Reduced CSF absorption at the arachnoidal villi - most common Head injury SAH Meningitis
75
Classic triad of normal pressure hydrocephalus
1. Urinary incontinence 2. Dementia and bradyphrenia 3. Gait abnormality (may be similar to PD)
76
Definition of bradyphrenia
Slowness of thought
77
How long a time period do the symptoms of hydrocephalus develop over?
Months
78
Investigations for normal pressure hydrocephalus
Imaging - enlarged 4th ventricle - ventriculomegaly - absence of substantial sulcal atrophy
79
Management of normal pressure hydrocephalus
Ventriculoperitoneal shunting
80
What % of patients with shunts experience significant complications and what are these complications?
10% Seizures Infection ICH
81
What is syringomyelia?
A collection of CSF within the spinal cord
82
Causes of syringomyelia
Chiari malformation (STRONG association) Trauma Tumours Idiopathic
83
Presentation of syringomyelia
Neck and arms loss of sensation to temp but preservation of light touch, proprioception and vibration Spastic weakness (predominantly of upper limbs) Paraesthesia Neuropathic pain Upgoing plantars Bowel and bladder dysfunction
84
What may occur over years if syringomyelia is not treated?
``` Scoliosis Horners syndrome (rare) ```
85
Investigations of syringomyelia
``` Full spine MRI (to exclude tumours or tethered cord) Brain MRI (chiari malformation) ```
86
Treatment of syringomyelia
Treat cause | If symptomatic or persistent - a shunt can be placed into it
87
Treatment of idiopathic intracranial hypertension
Acetazolamide
88
What does an isolated result of high protein in the CSF indicate?
Guillian barre syndrome
89
Types of cerebral oedema
Vasogenic Cytotoxic Interstitial
90
Pathology of vasogenic cerebral oedema
Increased capillary permeability
91
Causes of vasogenic cerebral oedema
Trauma Tumour Ischaemia Infarction
92
Causes of cytotoxic cerebral oedema
Hypoxia
93
Causes of interstitial cerebral oedema
Obstructive hydrocephalus | Hyponatraemia